Objective To characterize the production of the monoalthough in most patients there was a minor band of reactivity at 54 kDa. A panel of human bladder cancer cyte activation marker, soluble CD14 (sCD14), after bacille Calmette-Guérin (BCG) immunotherapy for cell lines did not react with the anti-CD14 monoclonal antibodies 3C10, 5C5 and BA8, and the antibodies superficial bladder cancer. Patients and methods Nineteen patients with carcinoma also failed to react with malignant epithelial cells in frozen sections of untreated bladder tumour. in situ were treated with a standard regimen of intravesical BCG. Urine samples were collected after each Furthermore, sCD14 was not secreted by cultured bladder tumour cells. The source of urinary sCD14 is instillation and analysed; the levels of soluble CD14 were determined by an enzyme-linked immunosorbent likely to be the resident and infiltrating macrophages in the bladder wall. Freshly isolated peripheral blood assay, the molecular weight confirmed by Western blotting and the possible cell source investigated using monocytes secreted sCD14 in response to BCG in a manner analogous to stimulation with bacterial lipoimmunohistochemistry.Results The mean levels of sCD14 were higher in polysaccharide. Conclusion A soluble form of CD14 is secreted into the patients with persistent carcinoma (designated as failures) than in those who had successful complete urine of patients who receive intravesical BCG. The measurement of soluble urinary CD14 could be of responses (responders) to BCG immunotherapy. The diÂerences were statistically significant, with P= prognostic significance for the response to immunotherapy. 0.034 at instillation 4 and P=0.027 at instillation 5 for the total mass of sCD14, and P=0.049 at instilKeywords Bacille Calmette-Guérin, BCG, lipopolysaccharide, bladder cancer, CD14 lation 4 for the concentration of sCD14. The predominant type of sCD14 in urine was the 48 kDa form, bladder wall is infiltrated by many neutrophils, lympho-

During the period 1967 to 1978, 1166 girls were admitted to our department because of urinary tract infection. In 97 of the 439 girls examined by cystoscopy, cystitis cystica was found. The age of the 97 girls varied from 3 to 12 years, mean 7 1/2 years. E. coli was found to be the major pathogenic organism in the urine. All but 3 girls had a history of recurrent urinary tract infection. Urinary tract abnormalities were found with the same frequency as in other studies concerning urinary tract infection in childhood. Vesicoureteric reflux was demonstrated on the cystogram for 33% of the girls. Patients with cystitis cystica are a hard core group requiring long-term treatment and follow-up. Different therapeutic methods are discussed and our experience with chlorhexidine bladder instillation is mentioned. The literature concerning cystitis cystica, especially in childhood, is also discussed.

Heart failure is the leading cause of death worldwide. Our focus is on non-genetic mechanisms by which cardiac regeneration can be lengthened or enhanced. Specifically, we are interested in the cyto-protective effects of glucose in cardiomyocyte growth, differentiation and proliferation and how this knowledge can be applied to regeneration therapies. Our preliminary data showed that glucose induces cardiomyocyte proliferation and inhibits cardiomyocyte maturation in human embryonic stem cells derived cardiomyocytes (hESC-CM) via the Pentose Phosphate Pathway in a dose dependent manner. Whether this pathway can be a therapeutic target for heart regeneration is unknown. Our hypothesis is that glucose promotes neonatal heart regeneration in a murine model. Non-Transmural cryoinjury was performed to the apex of the left ventricle in wild-type pups and cardiac specific overexpression of Glucose Transporter 1 Transgenic pups. In the acute phase (P1-P7), the level of cardiomyocyte cell proliferation was measured via flow cytometry analysis and immunostaining with PH3 and cTnnt. Glucose uptake by cardiomyocytes was measured by 18F-FDG assay and Glut1 immunostaining. In the chronic phase (P14, P21, P40), we quantified the level of fibrosis by histology (H&E and Picrosirius Red) and neovascularization by immunostaining with PECAM. Increased cardiomyocyte proliferation was observed in the Transgenic Glut1 pups. Myocardial glucose uptake declines from the muscular layer towards the trabecular layer, corresponding with maturation of the heart. We observed that Glut1 cardiomyocyte-specific overexpression resulted in improved cardiac repair compared to wild type (WT) mice at 21 days postnatally. Compared to wild-type, Glut1 hearts showed increased angiogenesis around the site of injury secondary to an increase in cardiomyocyte proliferation. This study is the first to demonstrate the potential role of glucose as a promoter for cardiac regeneration and reveal a potential mechanism for congenital cardiomyopathy associated with diabetic pregnancy.